Our results demonstrate that carcinomas resistant to hormonal manipulations still depend on the expression of the androgen receptor for their development in vivo

cDNA were used as a template, together with the pairs of oligonucleotides specified in the Functional Characterization of Yeast Ptc6 value: 1.51E-05). We also found 7 genes involved in ion transport. Taken together, the comparison of the phenotypic and transcriptomic data presented here, as well as the previously reported results suggest that the cellular functions of Ptc6 are substantially different from those of Ptc1 and also from Ptc2-Ptc5. Ptc6 and Ptc1 participate in the TOR signaling pathway by different mechanisms As previously described, the ptc1 strain is more sensitive to rapamycin than ptc6 cells. We show here that the double mutant ptc1 ptc6 was even more sensitive to this compound than ptc1 cells. Interestingly, the rapamycin-sensitive phenotype of ptc1 is not altered at all by further deletion of PTC2 or PTC3, which encode the closest structural relatives to Ptc1. The observation that the mutation of PTC6 in a ptc1 background is specific and additive suggests that Ptc1 and Ptc6 phosphatases could interact with the TOR pathway at different levels. It has been reported that certain vps mutants fail to recover from rapamycin-induced arrest. Since ptc1 shows diverse phenotypes alike to vps mutants we tested the ability to resume growth in rapamycin-treated ptc1 cells after the drug is removed. Functional Characterization of Yeast Ptc6 vacuolar hydrolases, which have been shown unable to SB-705498 chemical information degrade Aco1 when growing on lactate upon rapamycin incubation. Thus, cells lacking Ptc6 have an impaired mitophagy phenotype when treated with rapamycin in medium containing glucose as carbon source. Therefore, our results extend those reported by Tal and coworkers showing that Ptc6 was required for efficient mitophagy in prolonged stationary-phase incubation in medium containing lactate, a non-fermentable carbon source. Ptc6 is also required for the delay in Aco1 degradation observed in wild type cells treated with rapamycin in a non-fermentable carbon source such as glycerol. We next asked whether the ptc6 mutant would be similarly sensitive to rapamycin irrespectively of the carbon source. Interestingly, as shown in The rapamycin-sensitive phenotype of the ptc6 mutant is independent of the lack of PDH activity The only cellular target for Ptc6 described so far is Pda1, which is also dephosphorylated by Ptc5. As shown in deletion of PTC6 increased the rapamycin hypersensitive phenotype of tor1 cells, similarly to that observed for the deletion of PTC1. However, contrary to the previously observed for the ptc1 mutants, deletion of the PTC6 gene in the sit4 17496168 or tip41 backgrounds decreased the tolerance to the drug. Therefore, our data suggest that, in contrast to what happens in the case of ptc1, the sit4 and tip41 mutations are not epistatic to the ptc6 mutation. Therefore, taking together these results indicate that both Ptc6 23713790 and Ptc1 are involved in the normal functioning of the TOR signaling pathway but they are affecting different mechanisms. Rapamycin-induced mitophagy is blocked in ptc6 mutants growing on glucose One of the events controlled by the TOR signaling pathway, together with Ras-PKA signaling and the general stress response pathways, is mitophagy, a vacuole-dependent mitochondrial degradation process. Several circumstances have been described that lead to yeast mitophagy, including those that inhibit the TOR pathway, such as entry in stationary phase, nitrogen starvation or treatment with rapamycin. By following the degradatio